Gibberellic acid-induced changes in glutathione metabolism and anthocyanin content in plant tissue

Literature data point to a possible link between gibberellic acid (GA₃) and glutathione metabolism in plant tissue, as both are connected to dormancy breakage. In order to study the influence of GA₃ on glutathione metabolism, we treated an anthocyanin accumulating cell culture of periwinkle (Catharanthus roseus) and a shoot differentiated culture of pea (Pisum sativum) with GA₃. Glutathione reductase (GR; E.C. 1.6.4.2) activity increased to 135% and 190% of the control in C. roseus and P. sativum, respectively. The level of oxidized glutathione (GSSG) decreased to 60% of the control in the C. roseus culture while no change in GSSG was observed in the P. sativum culture. No changes in the tissue concentration of total glutathione was observed in the cultures after GA₃ treatment. Concomitant to the changes in GSSG and GR, an increase in anthocyanin accumulation was observed in the C. roseus culture in association with a strong increase in phenylalanine ammonia-lyase (PAL; E.C. 4.3.1.5) activity in response to GA₃. These data strongly suggest a link between GA₃ and glutathione metabolism.     

Oxidation of certain cyclic carbonyl compounds with alkaline hydrogen peroxide

The following cyclic compounds were oxidized at 4° by means of aqueous sodium peroxide in large excess: 2,3,4,6/5-pentahydroxycyclohexanone (1); xylo-pentahydroxy-2-cyclohexen-l-one (2); xylo-trihydroxycyclohexane-1,2,3-trione (3); reductic acid (4); and ninhydrin (5). On oxidation, 1, 2, and 3 gave carbon dioxide, formic acid, and oxalic acid; in addition, 1 yielded DL-glucaric acid, and 2 and 3 afforded xylaric acid. Compound 4 gave almost equimolecular quantities of carbon dioxide and succinic acid. In addition to a small amount of formic acid, compound 5 gave carbon dioxide and phthalic acid in yields of 92 and 95%, respectively. Reaction mechanisms are proposed.     

The stimulation of cerebral N2-methyl- and N2-2-dimethyl guanine-specific tRNA methyltransferases by methionine sulfoximine: an in vivo study.

The administration of a single convulsant dose or of multiple subconvulsant doses of L-methionine-dl-sulfoximine (MSO) to 18-day old rats results in a significant elevation of the specific activity of cerebral tRNA methyltransferases, as determined in an $\text{in vitro}$ assay, using heterologous or species-homologous tRNAs as substrates. The increase was detectable as early as 90 min after MSO and persisted throughout the entire 5–6 h preconvulsant period. The ¹⁴[C]-methyl tRNA was purified, and hydrolyzed to its constituent bases and their distribution was quantitated by high performance liquid chromatography. A marked increase in the formation of ¹⁴[C]-N²-methyl- and ¹⁴[C]-N₂²-dimethyl guanine was noted in the MSO-treated animals, demonstrating a specific stimulation by MSO $\text{in vivo}$ of the cerebral N²-methyl and/or N₂²-dimethyl guanine-specific tRNA methyltransferases.     

Prostaglandin inhibition of cyclic-AMP accumulation and rate of lipolysis in fat cells

A direct relationship between the rate of cyclic AMP accumulation for 2 minutes and the rate of free fatty acid mobilization for 20 minutes was found in rat isolated fat cells stimulated with norepinephrine or theophylline. The concentration-dependent inhibition of cAMP accumulation by prostaglandin E₂ was reflected in proportional inhibition of lipolysis. These data suggest that the anti-lipolytic mechanism of action of prostaglandin E₂ is mediated by inhibition of the early rate of cAMP accumulation rather than the total production of cAMP.     

DBA/2J Genetic Background Exacerbates Spontaneous Lethal Seizures but Lessens Amyloid Deposition in a Mouse Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is a leading cause of dementia in the elderly and is characterized by amyloid plaques, neurofibrillary tangles (NFTs) and neuronal dysfunction. Early onset AD (EOAD) is commonly caused by mutations in amyloid precursor protein (APP) or genes involved in the processing of APP including the presenilins (e.g. PSEN1 or PSEN2). In general, mouse models relevant to EOAD recapitulate amyloidosis, show only limited amounts of NFTs and neuronal cell dysfunction and low but significant levels of seizure susceptibility. To investigate the effect of genetic background on these phenotypes, we generated APP^swe and PSEN1^de9 transgenic mice on the seizure prone inbred strain background, DBA/2J. Previous studies show that the DBA/2J genetic background modifies plaque deposition in the presence of mutant APP but the impact of PSEN1^de9 has not been tested. Our study shows that DBA/2J.APP^swePSEN1^de9 mice are significantly more prone to premature lethality, likely to due to lethal seizures, compared to B6.APP^swePSEN1^de9 mice—70% of DBA/2J.APP^swePSEN1^de9 mice die between 2-3 months of age. Of the DBA/2J.APP^swePSEN1^de9 mice that survived to 6 months of age, plaque deposition was greatly reduced compared to age-matched B6.APP^swePSEN1^de9 mice. The reduction in plaque deposition appears to be independent of microglia numbers, reactive astrocytosis and complement C5 activity.     

Angiogenesis during human extraembryonic development involves the spatiotemporal control of PDGF ligand and receptor gene expression.

We have examined the role of platelet-derived growth factor (PDGF) ligand and receptor genes in the angiogenic process of the developing human placenta. In situ hybridization analysis of first trimester placentae showed that most microcapillary endothelial cells coexpress the PDGF-B and PDGF beta-receptor genes. This observation indicates that PDGF-B may participate in placental angiogenesis by forming autostimulatory loops in capillary endothelial cells to promote cell proliferation. Endothelial cells of macro blood vessels maintained high PDGF-B expression, whereas PDGF beta-receptor mRNA was not detectable. In contrast, PDGF beta-receptor mRNA was readily detectable in fibroblast-like cells and smooth muscle cells in the surrounding intima of intermediate and macro blood vessels. Taken together, these data suggest that the PDGF-B signalling pathway appears to switch from an autocrine to a paracrine mechanism to stimulate growth of surrounding PDGF beta-receptor-positive mesenchymal stromal cells. Smooth muscle cells of the blood vessel intima also expressed the PDGF-A gene, the protein product of which is presumably targeted to the fibroblast-like cells of the mesenchymal stroma as these cells were the only ones expressing the PDGF alpha-receptor. PDGF-A expression was also detected in columnar cytotrophoblasts where it may have a potential role in stimulating mesenchymal cell growth at the base of the growing placental villi. We discuss the possibility that the regulation of the PDGF-B and beta-receptor gene expression might represent the potential targets for primary angiogenic factors.